Inflammation is the major nonmechanical complication associated with implantation of intraocular lenses (IOL). The objective of the proposed research is to examine the mech;an;sm (s) whereby some patients with IOL implants develop protracted uveitis. Previous work by the applicant has established that nylon and polypropyleneloope IOLs activate the complement system in human serum. Activation of complemtn (C') results in the generation of biologically active peptides capable of provoking inflammation and tissue injury. The applicant now proposes to test the hypothesis that IOL components or aggregated proteins (immunolobulin G, IgG) adsorbed to the implant surface are cable of activating the C' system in aqueous humor (AH). Preliminary studies have demontrated small amounts of the third component of complement (C3) in normal AH (Cataract and eratoconus patients), higher levels of C3 in AH from patients with pseudophakic bullous keratopathy (PBK) and the presence of chemotactic activity in AH from PBK but not keratoconus patients. These studies will be expanded to determine whether IOL components activate the complement system in normal aqueous humor, whether AH from PBK patients contains complement derived proinflammatory peptides, and the mechanism(s) whereby complement derived proinflammatory peptides are generated by IOL. These studies should provide important clues both to the pathogenesis of the uveitis associated with IOL implatation as well as to possible "interventions" or modifications that can prevent or ameliorate IOL-induced inflammation.